Premium
Processed purple‐fleshed potato prevents and protects against high‐fat diet elevated oxidative stress and inflammation markers in vivo in a pig model
Author(s) -
Radhakrishnan Sridhar,
Kim Sung Woo,
Reddivari Lavanya,
Vanamala Jairam
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.862.21
Subject(s) - oxidative stress , inflammation , glutathione , in vivo , weaning , chemistry , antioxidant , oxidative phosphorylation , food science , medicine , endocrinology , biochemistry , biology , microbiology and biotechnology , enzyme
Little information exists if purple‐fleshed potatoes (PP), rich in anti‐oxidant and anti‐inflammatory anthocyanins, even after processing, retain their health benefiting properties in vivo. We hypothesized that processed PP will suppress high‐fat diet (HFD) elevated oxidative stress/inflammation biomarkers in a pig model. Thus, we performed two studies; a prevention study where 64 pigs, 3wk post‐weaning, consumed one of the eight diets; low‐fat (LFD), HFD and HFD supplemented with white‐fleshed potato (WP) or PP (raw/baked/chips; 10% w/w) for 13wk; and a protection study where pigs (12 wk on HFD) consumed HFD containing 10/20% PP or WP chips for additional 5wk (n=8). Both PP and WP diets (raw/baked/chips) suppressed urinary oxidative stress markers, 8‐isoprostane (8IP) and DNA adduct 8‐OHDG; and serum levels of TNF‐α (ELISA) compared to HFD control (P=0.038). Potato diets elevated colonic mucosal glutathione ratio (GSH:GSSG) compared to HFD control, however, greatest enhancement (P=0.046) was seen in raw PP consuming pigs. In the protection study, biomarkers of oxidative stress and inflammation, including colonic mucosal expression of COX‐2 and IFN‐γ (qRTPCR), and systemic levels of 8IP and TNF‐α were suppressed (P=0.049) by PP diets compared to control. These findings indicate that PP, even after processing, prevents and protects against HFD elevated colonic‐systemic oxidative stress/inflammation. Grant Funding Source : This work was supported by National Research Initiative Grant 2009–55200‐05197 from the USDA‐NIFA.